scholarly journals Structure-Activity Relationships of Lipopolysaccharide (LPS) in Tumor Necrosis Factor-.ALPHA. (TNF-.ALPHA.) Production and Induction of Macrophage Cell Death in the Presence of Cycloheximide (CHX) in a Murine Macrophage-Like Cell Line, J774.1.

1998 ◽  
Vol 21 (10) ◽  
pp. 1102-1105 ◽  
Author(s):  
Hisae KARAHASHI ◽  
Fumio AMANO
Keyword(s):  
Cell Death ◽  
Tumor Necrosis ◽  
Tnf Alpha ◽  
Murine Macrophage ◽  
Macrophage Cell ◽  
Necrosis Factor Alpha ◽  
Alpha Production ◽  
Structure Activity ◽  
Factor Alpha ◽  
Necrosis Factor

Role of lipopolysaccharide and tumor necrosis factor-alpha in induction of hepatocyte necrosis

1995 ◽  
Vol 269 (2) ◽  
pp. G297-G304 ◽  
Author(s):  
J. H. Wang ◽  
H. P. Redmond ◽  
R. W. Watson ◽  
D. Bouchier-Hayes
Keyword(s):  
Cell Death ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Acute Hepatic Failure ◽  
Tnf Alpha ◽  
Enzyme Release ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Necrosis Factor

The occurrence of acute hepatic failure during systemic inflammatory response syndrome (SIRS) is related to the extent of hepatocyte (HC) damage and cell death resulting from necrosis or apoptosis. We hypothesized that proinflammatory mediators such as lipopolysaccharide (LPS) and tumor necrosis factor-alpha (TNF-alpha) can, either directly or indirectly through neutrophil (PMN) and Kupffer cell (KC) activation, induce HC damage and cell death, and that the mechanism is cellular necrosis rather than apoptosis. The results in this study demonstrated that LPS and TNF-alpha alone and in combination are directly cytotoxic to cultured rat HC as indicated by the hepatocellular enzyme release and HC necrosis. However, LPS and TNF-alpha, in the presence of sodium arsenite (a heat shock inducer), were unable to induce HC apoptosis. Both KC and PMN activated by either LPS or TNF-alpha induced significant hepatocellular enzyme release and HC necrosis, which was dependent on the ratio of KC and PMN to HC. It is concluded that LPS and TNF-alpha may play a central role in the development of acute hepatic failure after severe trauma and sepsis by directly or indirectly inducing HC necrosis rather than apoptosis.

Macrophage Cell Activation with Acute Apical Abscess Contents Determined by Interleukin-1 Beta and Tumor Necrosis Factor Alpha Production

2014 ◽  
Vol 40 (11) ◽  
pp. 1752-1757 ◽  
Author(s):  
Ezilmara L.R. Sousa ◽  
Frederico C. Martinho ◽  
Fabio R.M. Leite ◽  
Gustavo G. Nascimento ◽  
Brenda P.F.A. Gomes
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Cell Activation ◽  
Interleukin 1 ◽  
Interleukin 1 Beta ◽  
Macrophage Cell ◽  
Necrosis Factor Alpha ◽  
Alpha Production ◽  
Factor Alpha ◽  
Necrosis Factor

scholarly journals Lipopolysaccharide-induced selective priming effects on tumor necrosis factor alpha and nitric oxide production in mouse peritoneal macrophages.

1993 ◽  
Vol 177 (2) ◽  
pp. 511-516 ◽  
Author(s):  
X Zhang ◽  
D C Morrison
Keyword(s):  
Tumor Necrosis ◽  
Peritoneal Macrophages ◽  
Tnf Alpha ◽  
No Production ◽  
Necrosis Factor Alpha ◽  
Priming Effects ◽  
Alpha Production ◽  
Factor Alpha ◽  
Mouse Peritoneal Macrophages ◽  
Necrosis Factor

Preculture of thioglycollate-elicited C3HeB/FeJ mouse peritoneal macrophages in vitro with subthreshold stimulatory concentrations of lipopolysaccharide (LPS) can induce hyporesponsiveness (desensitization) to both tumor necrosis factor alpha (TNF-alpha) and nitric oxide (NO) production when these cells are subsequently stimulated with 100 ng/ml of LPS. We have established, however, that the primary dose of LPS required for inducing downregulation of NO production is significantly lower than that required for inducing downregulation of TNF-alpha production. Further, when LPS-pretreated macrophages become refractory to subsequent LPS stimulation for NO production, the secondary LPS-stimulated TNF-alpha production is markedly enhanced, and vice versa. These results indicate that LPS-induced TNF-alpha and NO production by macrophages are differentially regulated, and that the observed desensitization process may not reflect a state in which macrophages are totally refractory to subsequent LPS stimulation. Rather, our data suggest that LPS-pretreated macrophages become selectively primed for differential responses to LPS. The LPS-induced selective priming effects are not restricted to LPS stimulation, but extend as well to stimuli such as zymosan, Staphylococcus aureus, and heat-killed Listeria monocytogenes.

scholarly journals Polymorphisms in the tumor necrosis factor alpha (TNF-alpha) gene correlate with murine resistance to development of toxoplasmic encephalitis and with levels of TNF-alpha mRNA in infected brain tissue.

1992 ◽  
Vol 175 (3) ◽  
pp. 683-688 ◽  
Author(s):  
Y R Freund ◽  
G Sgarlato ◽  
C O Jacob ◽  
Y Suzuki ◽  
J S Remington
Keyword(s):  
Brain Tissue ◽  
Tumor Necrosis ◽  
Toxoplasmic Encephalitis ◽  
Tnf Alpha ◽  
Necrosis Factor Alpha ◽  
Alpha Production ◽  
D Region ◽  
Factor Alpha ◽  
Alpha Gene ◽  
Necrosis Factor

Murine resistance to development of toxoplasmic encephalitis (TE) has recently been mapped to the D region of the major histocompatibility complex (H-2). Since the gene for tumor necrosis factor alpha (TNF-alpha) is located 5' of the D region and TNF-alpha has been implicated as playing a role in neurological diseases, we were interested in determining the relationship of TNF-alpha production to TE resistance. We have demonstrated that resistance to TE in inbred mice can be correlated with specific restriction fragment length polymorphisms and microsatellite variants in the TNF-alpha gene. Mice that are susceptible to TE express elevated levels of TNF-alpha mRNA in brain tissue 6 wk after infection with the ME49 strain of Toxoplasma gondii. Resistant mice and all mice that are uninfected show no detectable TNF-alpha mRNA expression in brain tissue. Differences in the TNF-alpha gene between susceptible and resistant mice have been localized to the first intron, the promoter, and the 3' end of the TNF-alpha gene. These data implicate differences in regulation of TNF-alpha production in brain tissue as contributing to differences in susceptibility to development of TE.

scholarly journals Macrophage priming and lipopolysaccharide-triggered release of tumor necrosis factor alpha during graft-versus-host disease.

1992 ◽  
Vol 175 (2) ◽  
pp. 405-413 ◽  
Author(s):  
F P Nestel ◽  
K S Price ◽  
T A Seemayer ◽  
W S Lapp
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Acute Gvhd ◽  
Tnf Alpha ◽  
Triggered Release ◽  
Necrosis Factor Alpha ◽  
Alpha Production ◽  
Factor Alpha ◽  
Necrosis Factor

In this report we have investigated macrophage (M phi) activity and tumor necrosis factor alpha (TNF-alpha) production during graft-vs.-host disease (GVHD). TNF-alpha production by M phi requires two signals: priming of M phi by interferon followed by triggering of TNF-alpha production and release by lipopolysaccharide (LPS). The state of M phi activation was examined in nonirradiated B6AF1 recipient mice injected with either 60 x 10(6) (acute GVHD) or 30 x 10(6) (nonlethal GVHD) parental B6 lymphoid cells. During the early phase of acute GVHD, administration of normally sublethal amounts of LPS-triggered release of significant amounts of TNF-alpha into the serum resulting in death of the animals within 36 h. Normal animals treated with the same dose of LPS neither died nor produced detectable amounts of serum TNF-alpha. In vitro studies demonstrated that M phi were primed during GVHD. The level of M phi priming was greater during acute GVHD than nonlethal GVHD since 100-fold less LPS was required to trigger killing of a TNF-alpha-sensitive cell line by M phi from acute GVHD animals. The amount of TNF-alpha released into the serum after LPS injection increased during the course of the GVHD and was significantly greater in acute GVH-reactive mice. Endogenous LPS was detected in the serum of acute GVH-reactive animals coincident with the onset of mortality. The data provide evidence that during GVHD M phi are primed as a result of the allogeneic reaction and that endogenous LPS therefore triggers M phi production of TNF-alpha resulting in the symptoms characteristic of acute GVHD.

Increased cell death in rat blastocysts exposed to maternal diabetes in utero and to high glucose or tumor necrosis factor-alpha in vitro

Development ◽  
1997 ◽  
Vol 124 (23) ◽  
pp. 4827-4836 ◽  
Author(s):  
S. Pampfer ◽  
I. Vanderheyden ◽  
J.E. McCracken ◽  
J. Vesela ◽  
R. De Hertogh
Keyword(s):  
Cell Death ◽  
Tumor Necrosis ◽  
Maternal Diabetes ◽  
Diabetic Rats ◽  
Tnf Alpha ◽  
Nuclear Fragmentation ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Necrosis Factor

The morphogenetic function of the transient phase of cell death that occurs during blastocyst maturation is not known but it is thought that its regulation results from a delicate balance between survival and lethal signals in the uterine milieu. In this paper, we show that blastocysts from diabetic rats have a higher incidence of dead cells than control embryos. Differential lineage staining indicated that increased nuclear fragmentation occurred mainly in the inner cell mass. In addition, terminal transferase-mediated dUTP nick end labeling (TUNEL) demonstrated an increase in the incidence of non-fragmented DNA-damaged nuclei in these blastocysts. Analysis of the expression of clusterin, a gene associated with apoptosis, by quantitative reverse transcription-polymerase chain reaction detected an increase in the steady-state level of its transcripts in blastocysts from diabetic rats. In situ hybridization revealed that about half the cells identified as expressing clusterin mRNA exhibited signs of nuclear fragmentation. In vitro experiments demonstrated that high D-glucose increased nuclear fragmentation, TUNEL labeling and clusterin transcription. Tumor necrosis factor-alpha (TNF-alpha), a cytokine whose synthesis is up-regulated in the diabetic uterus, did not induce nuclear fragmentation nor clusterin expression but increased the incidence of TUNEL-positive nuclei. The data suggest that excessive cell death in the blastocyst, most probably resulting from the overstimulation of a basal suicidal program by such inducers as glucose and TNF-alpha, may be a contributing factor of the early embryopathy associated with maternal diabetes.

scholarly journals Induction of tumor necrosis factor alpha production by human hepatocytes in chronic viral hepatitis.

1994 ◽  
Vol 179 (3) ◽  
pp. 841-848 ◽  
Author(s):  
R González-Amaro ◽  
C García-Monzón ◽  
L García-Buey ◽  
R Moreno-Otero ◽  
J L Alonso ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Kupffer Cells ◽  
Human Liver ◽  
Tumor Necrosis ◽  
Tnf Alpha ◽  
Necrosis Factor Alpha ◽  
Alpha Production ◽  
Factor Alpha ◽  
Necrosis Factor

Tumor necrosis factor alpha (TNF-alpha) is a multifunctional cytokine that has an important role in the pathogenesis of inflammation, cachexia, and septic shock. Although TNF-alpha is mainly produced by macrophages, there is evidence regarding TNF-alpha production by cells that are not derived from bone marrow. TNF-alpha production by normal and inflamed human liver was assessed at both mRNA and protein levels. Using a wide panel of novel anti-TNF-alpha monoclonal antibodies and a specific polyclonal antiserum, TNF-alpha immunoreactivity was found in hepatocytes from patients chronically infected with either hepatitis B virus (HBV) or hepatitis C virus. Minimal TNF-alpha immunoreactivity was detected in the mononuclear cell infiltrate and Kupffer cells. In situ hybridization experiments using a TNF-alpha RNA probe showed a significant expression of TNF-alpha mRNA in hepatocytes, Kupffer cells, and some infiltrating mononuclear cells. By contrast, TNF-alpha was detected at low levels in liver biopsies from normal individuals or patients with alcoholic liver disease and low expression of TNF-alpha mRNA was observed in these specimens. Transfection of HepG2 hepatoblastoma cells with either HBV genome or HBV X gene resulted in induction of TNF-alpha expression. Our results demonstrate that viral infection induces, both in vivo and in vitro, TNF-alpha production in hepatocytes, and indicate that the HBV X protein may regulate the expression of this cytokine. These findings suggest that TNF-alpha may have an important role in human liver diseases induced by viruses.

scholarly journals Selective inhibition of spontaneous IgE and IgG4 production by interleukin-8 in atopic patients

Blood ◽  
1995 ◽  
Vol 85 (11) ◽  
pp. 3191-3198 ◽  
Author(s):  
H Kimata ◽  
I Lindley ◽  
K Furusho
Keyword(s):  
Monoclonal Antibody ◽  
B Cells ◽  
Tumor Necrosis ◽  
Selective Inhibition ◽  
Tnf Alpha ◽  
Necrosis Factor Alpha ◽  
Endogenous Production ◽  
Alpha Production ◽  
Factor Alpha ◽  
Necrosis Factor

The effects of interleukin (IL)-8 on spontaneous IgE and IgG4 production in atopic patients were studied. IL-8 inhibited IgE and IgG4 production by purified surface (s) IgE+ and sIgG4+ B cells, respectively, while it had no effect on IgG1, IgG2, IgG3, IgM, IgA1, and IgA2 production by corresponding sIg+ B cells. The IL-8-induced inhibition was counteracted by IL-6 and tumor necrosis factor-alpha (TNF-alpha) and was blocked by anti-IL-8 monoclonal antibody (MoAb). Conversely, the addition of anti-IL-6 MoAb and anti-TNF-alpha MoAb, in the absence of IL-8, inhibited IgE and IgG4 production by sIgE+ and sIgG4+ B cells, respectively. Purified sIgE+ and sIgG4+ B cells expressed IL-6 receptors (R), TNF-alpha R, and IL-8R, and they produced IL-6 and TNF-alpha, but not IL-8. IL-8 had no effect on IL-6R or TNF- alpha R, while it abrogated IL-6 and TNF-alpha production in these cells. In contrast, slgG1+, slgG2+, slgG2+, slgG3+, slgM+, slgA1+, and slgA2+ B cells expressed IL-6R and TNF-alpha R but not IL-8R, and they produced IL-6 and TNF-alpha. IL-8 had no effect on IL-6R and TNF-alpha R, or on TNF-alpha and IL-6 production in these cells. These results indicate that IL-8 inhibits spontaneous IgE and IgG4 production in slgE+ and slgG4+ B cells, respectively, by inhibiting the endogenous production of IL-6 and TNF-alpha.

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